KHOẢNG TRỐNG GLYCAT HÓA VÀ CHỈ SỐ GLYCAT HÓA HEMOGLOBIN TRONG BỆNH THẬN DO ĐÁI THÁO ĐƯỜNG TÍP 2: CƠ SỞ SINH LÝ BỆNH, BẰNG CHỨNG LÂM SÀNG VÀ TRIỂN VỌNG ỨNG DỤNG

Abstract

Objective: To synthesize the pathophysiological basis, methods of determination and clinical evidence for the glycation gap (GG) and the hemoglobin glycation index (HGI) in type 2 diabetic kidney disease. Methods: A structured narrative review. PubMed/MEDLINE, the Cochrane Library, Google Scholar and the official American Diabetes Association and KDIGO websites were searched up to 31 July 2026, with predefined inclusion and exclusion criteria and an author-assigned risk-of-bias rating for each study. Results: GG and HGI are residual indices, calculated as measured HbA1c minus HbA1c predicted from fructosamine or from glucose. Both may reflect the combined influence of several biological and measurement-related sources of variation rather than hemoglobin glycation alone, and both depend on a population-specific regression equation, so values are not directly comparable across studies. Cross-sectional studies report associations of a higher GG or HGI with albuminuria and prevalent kidney disease. In type 2 diabetes, a 5-year cohort found a 58% higher risk of renal progression in the highest tertile of first-year mean HGI (HR 1.58; 95% CI 1.01-2.49), whereas a 1,050-patient cohort described a U-shaped association with incident nephropathy. Incremental predictive value beyond HbA1c, the urinary albumin-to-creatinine ratio and estimated glomerular filtration rate has not been established. Anemia, altered erythrocyte turnover, erythropoiesis-stimulating therapy, hypoalbuminemia and proteinuria may all bias the indices. Conclusion: GG and HGI may help interpret an HbA1c value that is discordant with directly measured glucose. Current evidence does not support their independent use for diagnosis, renal risk stratification or adjustment of treatment.